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001-es BibID:BIBFORM087277
Első szerző:Douida, Abdennour
Cím:The proteasome activator PA200 regulates expression of genes involved in cell survival upon selective mitochondrial inhibition in neuroblastoma cells / Abdennour Douida, Frank Batista, Agnieszka Robaszkiewicz, Pal Boto, Azzam Aladdin, Mónika Szenykiv, Rita Czinege, László Virág, Krisztina Tar
Dátum:2020
ISSN:1582-1838 1582-4934
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Journal Of Cellular And Molecular Medicine. - 24 : 12 (2020), p. 6716-6730. -
További szerzők:Batista, Frank (1975-) (biokémikus) Robaszkiewicz, Agnieszka (1983-) (biokémikus) Botó Pál (1986-) (molekuláris biológus) Aladdin, Azzam (1980-) (molekuláris biológus) Szenykiv Mónika Czinege Rita Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Tar Krisztina (1975-) (biokémikus, molekuláris biológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00020
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GINOP-2.3.2-15-2016-00048
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OTKA K112336
OTKA
OTKA K132193
OTKA
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2.

001-es BibID:BIBFORM048850
035-os BibID:PMID:23722590
Első szerző:Erdélyi Katalin (molekuláris biológus, biokémikus)
Cím:Role of poly(ADP-ribosyl)ation in a 'two-hit' model of hypoxia and oxidative stress in human A549 epithelial cells in vitro / Katalin Erdélyi, Pál Pacher, László Virág, Csaba Szabó
Dátum:2013
ISSN:1107-3756
Megjegyzések:A preceding hypoxic insult can sensitize the cells or the organism to a subsequent, second insult. The aim of the present study was to investigate the molecular mechanism of this phenomenon (often termed 'two-hit' injury paradigm), in an in vitro model of hypoxia/oxidative stress injury in A549 epithelial cells, with special emphasis on the role of the nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP-1) in the process. Pre-exposure of the cells to 24 h hypoxia significantly reduced intracellular glutathione (GSH) levels, reduced mitochondrial activity and adenosine triphosphate (ATP) levels. However pre-exposure to hypoxia failed to induce any change in PARP-1 expression and activation, DNA single-strand breaks or plasma membrane integrity. Pre-exposure to hypoxia markedly increased the sensitivity of the cells to subsequent oxidative stress-induced DNA damage. Hydrogen peroxide (H2O2) induced a concentration-dependent increase in DNA breakage, PARP activation, depletion of intracellular ATP, inhibition of mitochondrial activity and two distinct parameters that quantify the breakdown of plasma membrane integrity (propidium iodide uptake or lactate dehydrogenase release). PARP-1 activation played a significant role in the H2O2-induced cell death response because PARP activation, depletion of intracellular ATP, inhibition of mitochondrial activity, and the breakdown of plasma membrane integrity were attenuated in cells with permanently silenced PARP-1. Based on measurement of the endogenous antioxidant GSH, we hypothesized that the mechanism of hypoxia-mediated enhancement of H2O2 involves depletion of the GSH during the hypoxic period, which renders the cells more sensitive to a subsequent DNA single-strand break elicited by H2O2. DNA strand breakage then activates PARP-1, leading to the inhibition of mitochondrial function, depletion of ATP and cell necrosis. PARP-1 deficiency protects against the cytotoxicity, to a lesser degree, by protecting against GSH depletion during the hypoxic period, and, to a larger degree, by maintaining mitochondrial function and preserving intracellular ATP levels during the subsequent oxidative stress period.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:International Journal of Molecular Medicine. - 32 : 2 (2013), p. 339-346. -
További szerzők:Pacher Pál Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Szabó Csaba
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3.

001-es BibID:BIBFORM028371
Első szerző:Komjáti Katalin
Cím:Poly(ADP-ribose) polymerase inhibition protect neurons and the white matter and regulates the translocation of apoptosis-inducing factor in stroke / Katalin Komjáti, John G. Mabley, László Virág, Garry J. Southan, Andrew L. Salzman, Csaba Szabó
Dátum:2004
ISSN:1107-3756
Megjegyzések:Focal cerebral ischemia activates the nuclear protein poly(ADP-ribose) polymerase (PARP). Apoptosis-inducing factor (AIF) is a flavoprotein that is normally confined to the mitochondria, but translocates to the nucleus, as shown by in vitro models of neuronal injury. Using INO-1001, a novel potent inhibitor of PARP, we determined the role of PARP activation in the process of AIF translocation in a rat model of focal cerebral ischemia. The potency of INO-1001 as a PARP inhibitor and its cytoprotective potential in oxidant-challenged human neuronal SK-N-MC cells was first confirmed in vitro. PARP inhibition markedly reduced infarct size and improved neurological status in both transient and permanent models of MCA occlusion in Sprague-Dawley rats, with a therapeutic window of 6 h and 2 h in the transient and permanent ischemia models, respectively. The PARP inhibitor reduced the accumulation of poly(ADP-ribose) in the ischemic/reperfused hemisphere and reduced the accumulation of APP in the white matter of the affected hemisphere, consistently with protection against neuronal necrosis and axonal damage, respectively. Immunohistochemical analysis showed the appearance of AIF labeling in neuronal nuclei of the border zone ischemic area in the striatum after stroke. Cytoplasmatic (axonal) AIF staining was significantly diminished in the necrotic core of the striatum, while it was somewhat enhanced at the borderline ischemic territories of the white matter. Inhibition of PARP with INO-1001 reshifted the location of the apoptotic marker to the axons in the ipsilateral striatum. Thus, PARP inhibition is neuroprotective and regulates the ischemic nuclear translocation of AIF in stroke.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:International Journal Of Molecular Medicine 13 : 3 (2004), p. 373-382. -
További szerzők:Mabley, Jon G. Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Southan, Garry J. Salzman, Andrew L. Szabó Csaba (1967-) (orvos)
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4.

001-es BibID:BIBFORM028390
Első szerző:Soriano, Francisco Garcia
Cím:Diabetic endothelial dysfunction : role of reactive oxygen and nitrogen species production and poly(ADP-ribose) polymerase activation / Francisco Garcia Soriano, László Virág, Csaba Szabó
Dátum:2001
ISSN:0946-2716
Megjegyzések:Peroxynitrite and hydroxyl radicals are potent initiators of DNA single-strand breakage, which is an obligatory stimulus for the activation of the nuclear enzyme poly(ADP ribose) polymerase (PARP). In response to high glucose incubation medium in vitro, or diabetes and hyperglycemia in vivo, reactive nitrogen and oxygen species generation occurs. These reactive species trigger DNA single-strand breakage, which induces rapid activation of PARP. PARP in turn depletes the intracellular concentration of its substrate, NAD+, slowing the rate of glycolysis, electron transport, and ATP formation. This process results in acute endothelial dysfunction in diabetic blood vessels. Accordingly, inhibitors of PARP protect against endothelial injury under these conditions. In addition to the direct cytotoxic pathway regulated by DNA injury and PARP activation, PARP also appears to modulate the course of inflammation by regulating the activation of nuclear factor kappaB, and the expression of a number of genes, including the gene for intercellular adhesion molecule 1 and the inducible nitric oxide synthase. The research into the role of PARP in diabetic vascular injury is now supported by novel tools, such as new classes of potent inhibitors of PARP and genetically engineered animals lacking the gene for PARP. Pharmacological inhibition of PARP emerges as a potential approach for the experimental therapy of diabetic vascular dysfunction.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
free radicals
oxidatns
nitric oxide
diabetes vascular
cytokine
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal of Molecular Medicine 79 : 8 (2001), p. 437-448. -
További szerzők:Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Szabó Csaba (1967-) (orvos)
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5.

001-es BibID:BIBFORM001035
Első szerző:Zákány Róza (anatómus-, kötőszövetbiológus)
Cím:Oxidative stress-induced poly(ADP-ribosyl)ation in chick limb bud-derived chondrocytes / Zákány R., Bakondi E., Juhász T., Matta C., Szíjgyártó Zs., Erdélyi K., Szabó E., Módis L., Virág L., Gergely P.
Dátum:2007
Megjegyzések:Oxidative stress has been implicated in the pathogenesisof various diseases affecting chondrogenesis or the function of articular cartilage. DNA damage caused byoxidative stress may trigger the activation of the nuclearenzyme, poly(ADP-ribose) polymerase-1 (PARP-1) whichmay contribute to tissue injury. We aimed at investigating the effects of peroxynitrite (100-600 ?M) and hydrogen peroxide (0.1-4 mM) on PARP activation and extracellular matrix production of high density micromass cultures (HDC)prepared from chick limb bud mesenchymal cells. We foundthat both oxidative species strongly inhibited matrix formation of HDCs treated on day 2 but not on day 5. The PARP inhibitor 3-aminobenzamide (3-AB) stimulated matrix production in non-stressed cells and prevented suppressed matrix production in oxidatively stressed cells. Both hydrogen peroxide and peroxynitrite induced PARP activation and poly(ADP-ribose) accumulation. Decreased proliferation, viability and NAD+ content were not or only slightly improved by 3-AB, indicating that 3-AB directly affects matrix formation. In conclusion, oxidative stress stimulates poly(ADP-ribose) metabolism and inhibits extracellular matrix production of HDCs in a PARP-dependent manner. Our findings may have implications for potential therapeutic approaches aimed at restoring the matrix production capacity of chondrogenic cells.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
poly(ADP-ribosyl)ation
oxidative stress
peroxynitrite
egyetemen (Magyarországon) készült közlemény
extracellular matrix
chondrocyte
Megjelenés:International Journal of Molecular Medicine. - 19 : 4 (2007), p. 597-605. -
További szerzők:Bakondi Edina (1975-) (biokémikus, vegyész) Juhász Tamás (1976-) (biológus, orvosbiológus) Matta Csaba (1980-) (molekuláris biológus, genetikus, angol szakfordító) Szíjgyártó Zsolt (1978-) (vegyész) Erdélyi Katalin (1978-) (molekuláris biológus, biokémikus) Szabó Éva (1965-) (bőrgyógyász, kozmetológus) Módis László (1939-) (anatómus, kötőszövetbiológus) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Gergely Pál (1947-) (biokémikus)
Internet cím:elektronikus változat
elektronikus változat
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6.

001-es BibID:BIBFORM028438
Első szerző:Zingarelli, Basilia
Cím:Oxidation, tyrosine nitration and cytostasis induction in the absence of inducible nitric oxide synthase / Zingarelli B., Virág L., Szabó A., Cuzzocrea S., Salzman A. L., Szabó Cs.
Dátum:1998
ISSN:1107-3756
Megjegyzések:In the present study, we evaluated the impact of the lack of the gene for inducible nitric oxide synthase (iNOS) on oxidation, tyrosine nitration and cytotoxicity reactions triggered by immunostimulation. In mice injected with E. coli endotoxin (bacterial lipopolysaccharide, LPS, 50 mg/kg i.p.), there was a significant increase in the degree of oxidation of dihydrorhodamine 123 to rhodamine 123. This response was attenuated by inhibition of NO biosynthesis with NG-methyl-L-arginine (L-NMA, 30 mg/kg i.p.). In mice lacking functional iNOS gene (iNOS knock-out mice), the degree of the LPS-induced, L-NMA inhibitable increase in dihydrorhodamine oxidation was decreased, but not completely abolished. LPS stimulation induced a marked increase in the immunoreactivity for nitrotyrosine (an indicator of peroxynitrite formation), as measured in the aorta and lung. An L-NMA inhibitable increase in nitrotyrosine staining induced by LPS was also observed in the tissues of the iNOS knockout animals. LPS treatment induced the appearance of DNA single strand breakage and a suppression of mitochondrial respiration in peritoneal macrophages ex vivo. A significant degree of LPS-induced DNA single strand breakage and suppression of mitochondrial respiration was still observed in the peritoneal macrophages obtained from the iNOS knockout animals. Macrophages from wild-type mice stimulated with LPS and interferon-gamma suppressed the proliferation of various target cells (P815 mastocytoma, L929 fibrosarcoma and embryonic lung fibroblast cell line): this effect was abolished by in vitro treatment with L-NMA (1 mM). Macrophages from the iNOS knockout animals exhibited a reduced degree of target cell cytostatic activity. The remainder of the cytostasis in iNOS knockout macrophages was abolished by preventing cell contact and neutralizing tumor necrosis factor á. The present results demonstrate that the lack of iNOS gene does not fully abolish oxidation, tyrosine nitration and cytostatic activity in response to immunostimulation. The current findings may have implications for the development of NO-based approaches for the experimental therapy of inflammation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:International Journal Of Molecular Medicine 1 : 5 (1998), p. 787-795. -
További szerzők:Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Szabó A. Cuzzocrea, Salvatore Salzman, Andrew L. Szabó Csaba (1967-) (orvos)
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